Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Stem cell factor (SCF) is a growth factor with multiple activities which acts on numerous cell types including primordial germ cells, haemopoietic stem cells, melanocytes and mast cells. SCF is critical for the development of the mast cell hyperplasia associated with infection with the intestinal parasites Nippostrongylus brasiliensis and Trichinella spiralis. In the present study we have assessed the role of SCF in the mast cell and eosinophil responses to Schistosoma mansoni in the rat by blocking its effects in vivo with polyclonal antibody to SCF. Rats treated with sheep anti-SCF antibody on days 21, 24, 27 and 30 of infection with S. mansoni showed a rapid decrease in serum concentrations of the mucosal mast cell-associated protease rat mast cell protease II (RMCP II) by day 24, compared with normal sheep IgG-treated controls. Similarly, the number of mucosal mast cells and RMCP II levels in both small intestine and liver were also significantly reduced by day 32 of infection. In contrast with the depeletion of mast cells and mast cell proteases, eosinophil numbers in liver or intestine did not change significantly after anti-SCF treatment compared with controls. These results confirm that mast cell survival and hyperplasia are dependent on the presence of SCF whilst demonstrating that the eosinophil recruitment to liver and intestine associated with S. mansoni infection is SCF-independent.
 ...
PMID:Stem cell factor dependent hyperplasia of mucosal-type mast cells but not eosinophils in Schistosoma mansoni-infected rats. 881 6

Expulsion of the gastrointestinal nematode Trichinella spiralis is associated with pronounced mastocytosis mediated by a Th2-type response involving IL-4, IL-10, and IL-13. Here we demonstrate that IL-18 is a key negative regulator of protective immune responses against T. spiralis in vivo. IL-18 knockout mice are highly resistant to T. spiralis infection, expel the worms rapidly and subsequently develop low levels of encysted muscle larvae. The increased speed of expulsion is correlated with high numbers of mucosal mast cells and an increase in IL-13 and IL-10 secretion. When normal mice were treated with rIL-18 in vivo, worm expulsion was notably delayed, and the development of mastocytosis and Th2 cytokine production was significantly reduced. The treatment had no effect on intestinal eosinophilia or goblet cell hyperplasia but specifically inhibited the development of mastocytosis. Addition of rIL-18 to in vitro cultures of bone marrow-derived mast cells resulted in a significant reduction in cell yields as well as in the number of IL-4-secreting mast cells. In vivo treatment of T. spiralis-infected IFN-gamma knockout mice with rIL-18 demonstrated that the inhibitory effect of IL-18 on mastocytosis and Th2 cytokine secretion is independent of IFN-gamma. Hence, IL-18 plays a significant biological role as a negative regulator of intestinal mast cell responses and may promote the survival of intestinal parasites in vivo.
 ...
PMID:IL-18 regulates intestinal mastocytosis and Th2 cytokine production independently of IFN-gamma during Trichinella spiralis infection. 1219 25

Expulsion of the gastro-intestinal nematode Trichinella spiralis is associated with a pronounced mastocytosis mediated by a T helper (Th) 2 type response involving interleukin (IL)-4 and IL-13. Here we demonstrate that IL-10 is a key regulator of protective immune responses against T. spiralis in vivo. IL-10 knockout mice or normal mice treated with a neutralizing anti-IL-10 receptor antibody are highly susceptible to a primary T. spiralis infection and show significantly delayed adult worm expulsion. Depletion of IL-10 resulted in elevated Th1 and Th2 cytokine responses but significantly reduced numbers of mucosal mast cells in the jejunum. Interestingly, the increase in IFN-gamma detected in the absence of IL-10 resulted in increased immunity to larval stages. Hence, IL-10 has a negative effect on immunity to the tissue dwelling larval stages of T. spiralis but plays a significant biological role as an in vivo regulator of intestinal mast cell responses and is crucially involved in protection against adult stages of intestinal parasites in vivo.
 ...
PMID:Contrasting roles for IL-10 in protective immunity to different life cycle stages of intestinal nematode parasites. 1293 14

Expulsion of the gastrointestinal nematode Trichinella spiralis is associated with a pronounced mastocytosis mediated by a Th2-type response involving IL-4, IL-10, and IL-13. When exogenous rIL-12 was administered to T. spiralis-infected NIH mice, this resulted in significant suppression of intestinal mast cell responses, delayed worm expulsion, increased muscle larvae burdens, and a transient, but significant decrease in early Th2 cytokine secretion. rIL-12 treatment also altered chemokine expression in the jejunal mucosa. The effects of exogenous IL-12 administration were largely independent of IFN-gamma as shown by rIL-12 treatment of IFN-gamma knockout mice. Hence, IL-12 may play a significant biological role as a direct negative regulator of intestinal Th2 responses and may act to promote the survival of intestinal parasites in vivo also in the absence of IFN-gamma.
 ...
PMID:IFN-gamma-independent effects of IL-12 during intestinal nematode infection. 1450 Jun 67

The present study aimed to clarify the role of mast cells in colitis with relapse induced in Wistar rats by trinitrobenzenosulphonic acid. Colitis induction increased the histamine concentration in the colon, which peaked on day 26. The number of mast cells, probably immature, was ten times higher on day 8. Different from animals infected with intestinal parasites, after colitis remission, mast cells do not migrate to the spleen, showing that mast cell proliferation presents different characteristics depending on the inflammation stimuli. Treatment with sulfasalazine, doxantrazole, quercetin, or nedocromil did not increase the histamine concentration or the mast cell number in the colon on day 26, thereby showing absence of degranulation of these cells. In conclusion, although mast cell proliferation is associated with colitis, these cells and their mediators appear to play no clear role in the colitis with relapses.
 ...
PMID:Relationship between mast cells and the colitis with relapse induced by trinitrobenzesulphonic acid in Wistar rats. 1943 63